Introduction: Transcatheter aortic valve implantation (TAVI) has emerged as an important treatment opti-on for patients with severe aortic stenosis and a high surgical risk. Atrial fibrillation has been identified as a predictor of worse outcomes through its thrombogenic nature and increased risk of embolic stroke. Therefore, these patients need chronic oral anticoagulation (OAC) for reducing the throboembolic events. Given that the typical patient who undergoes TAVI is elderly and frail, anticoagulation adds layers of complexity, increasing the risk of bleeding and hemorrhagic stroke.
Case presentation: We present the case of a 63 years old patient post-TAVI, with atrial flutter and a history of atrial fibrilation, with chronic lymphocytic leukae-mia, chronic anemia (beta talassemia) and nevertheless a history of hemorrhagic syndrom (upper gastrointes-tinal hemorrhage, epistaxis).
On admission, the patient was hemodynamically stable (BP=130/80 mmHg, AV=80/min). The heart sounds were arrhythmic and a systolic 2/6 murmur in the aortic area without irradiation on the carotid arteries was present. The electrocardiogram documented atrial fibrillation with a mean ventricular rate of 90/ min, major right bundle branch block and anterior left hemiblock. The echocardiography revealed an undila-ted left ventricle, with normal global systolic function (EF=59%), but with interventricular septal dyskinesia. The aortic biological prostheses was normofunctional. Biochemically, the INR was in the therapeutic range, under treatment with Acenocumarol. We mention that the patient was under dual antiplatelet therapy with Clopidogrel 75 mg/day and Aspenter 75 mg/day. During hospitalization, the patient presented a major 48-hour long epistaxis episode which required multiple haemostasis. We initially opted for discontinuation of the antiplatelet therapy while maintaining the antico-agulation with Acenocumarol, the patient presenting a therapeutic INR at the lower limit (2.05). Subsequently, because of the still ongoing bleeding, we replaced Acenocoumarol with low molecular weight heparin (HGMM) until bleeding stopped. 24 hours after hae-mostasis we reintroduced Acenocoumarol under rigo-rous control of INR.
Conclusions: Thus, in a patient with dual antiplatelet therapy post-TAVI and chronic oral anticoagulation for atrial flutter, but with a history of hemorrhagic syndro-me and beta thalassemia, who experienced an episode of epistaxis on the current admission, we preferred to discontinue the antiplatelet therapy while maintaining anticoagulation under careful control of INR. Evoluti-on was favorable.